ACTA ENDOCRINOLOGICA (BUC)

Introduction. Induction of heme oxygenase (HO) gene expression can protect lungs from Hypoxic Pulmonary\r\nVasoconstriction (HPV). Furthermore, there is evidence that Rho-kinase (ROCK) may be involved in HPV. Studies are going on to detect the real mechanisms involved in the phenomenon. Ghrelin, a 28-amino-acid peptide, has been shown that it may protect lungs from HPV side effects. The aim of this study was to evaluate the effect of exogenous ghrelin on HO and ROCK isoforms gene expression during chronic hypoxia (CH).\r\nMaterial and Method.Twenty four adult male Wistar rats were divided randomly in three groups. Hypoxic rats with saline or ghrelin treatment were placed in a normobaric hypoxic chamber (O2 11%), for two weeks. Controls remained in room air. HO and ROCK isoforms gene expression was measured by Real-Time RT-PCR. Lung tissues were histologically processed and stained with hematoxylin-eosin for morphometric analysis.\r\nResults. Morphometric analysis showed that ghrelin reversed the hypoxia induced pulmonary artery wall thickness (P < 0.001). In hypoxic animals, the amount of HO-1 expression increased but there was suppression in HO-2 gene expression (P < 0.05). Both ROCK-1 and ROCK-2 gene expressions were diminished after two-week hypoxia. Ghrelin treatment reduced the overexpression of HO-1 (P < 0.05), but had noeffect on ROCK gene expression.\r\nConclusion. Ghrelin by decreasing the expression of HO-1 and HO-2 in hypoxic animals may be involved in an adaptation\r\nmechanism during CH. However, ghrelin did not change ROCK isoforms gene expression, thus it could not affect HPV in this way. Nevertheless, more studies are needed to justify the protective roles of ghrelin for HPV.

Introduction. Menopause increases the risk of cardiovascular disease in women. The aims of the present study were to evaluate the effects of swimming training on cardiac histology and expression of miR-29 and IGF-1 in the ovariectomized rats. Materials and methods. Thirty female Wistar rats were divided into sham and ovariectomized groups: sedentary control (OVX) and trained with 8 weeks exercise (OVX.E). On 57th day, blood was collected and used for lipid profile measurement. In addition, heart tissue was analyzed by reverse transcription–polymerase chain reaction for IGF- 1 mRNA and miR-29, and studied for histopathological changes. Results. Ovariectomy significantly decreased miR- 29 and IGF-1 expression in the heart compared to sham animals group (p<0.05). Exercise training increased miR-29 and IGF- 1 expression in the trained rats and improved histology and lipid profile compared with OVX group (p<0.05). Conclusion. Estrogen deficiency could lead to cardiac fibrosis through deregulation miR-29 and IGF-1 expression. The findings of the current study suggests a protective effect of exercise on heart against fibrotic changes in ovariectomized rats and support a potential preventive value of exercise in improving cardiac function after menopause.